Mapping the vascular complications of acute pancreatitis: focus on splanchnic vein thrombosis.

We conducted a retrospective observational study analyzing 402 medical records from patients hospitalized with AP at a single tertiary-care university hospital between January 2018 and December 2023. The study included all adult patients (≥ 16 years old) who met at least two of the three established diagnostic criteria for AP: Abdominal pain consistent with AP. Serum lipase levels ≥ 3 times the upper limit of normal (ULN). Imaging findings (computed tomography [CT] or magnetic resonance imaging [MRI]) confirming the diagnosis of AP. Abdominal pain consistent with AP. Serum lipase levels ≥ 3 times the upper limit of normal (ULN). Imaging findings (computed tomography [CT] or magnetic resonance imaging [MRI]) confirming the diagnosis of AP. All patients underwent cross-sectional imaging at least 72 h after symptom onset, ensuring the detection of pancreatic and vascular complications. MRI was performed only when CT was contraindicated (e.g., due to contrast allergy or renal impairment). Exclusion criteria included: Patients with incomplete demographic information or missing follow-up data. Patients with underlying thromboembolic diseases (cirrhosis, myeloproliferative disorders, cancer) : based on a standardized screening approach including (1) review of prior medical records, (2) evaluation of previous CT/MRI imaging when available, (3) and documented hematologic disorders. Patients receiving anticoagulant therapy prior to AP diagnosis. Patients with incomplete demographic information or missing follow-up data. Patients with underlying thromboembolic diseases (cirrhosis, myeloproliferative disorders, cancer) : based on a standardized screening approach including (1) review of prior medical records, (2) evaluation of previous CT/MRI imaging when available, (3) and documented hematologic disorders. Patients receiving anticoagulant therapy prior to AP diagnosis. We focused on assessing the prevalence of SVT in AP and evaluating its significance in relation to patient prognosis as well as the management strategies employed (Fig.  1 ). Fig. 1 Flow chart for study participants Flow chart for study participants AP severity classification: Severity was assessed using validated scoring systems [ 7 ]: a- Revised Atlanta Classification of acute pancreatitis severity [ 8 ]. Mild AP (MAP): No organ failure or local/systemic complications; typically resolves within a week. Moderately Severe AP (MSAP): Characterized by transient organ failure (lasting less than 48 h), local complications, or exacerbation of coexisting diseases. Severe AP (SAP): Defined by persistent organ failure lasting 48 hours or more. Revised Atlanta Classification of acute pancreatitis severity [ 8 ]. Mild AP (MAP): No organ failure or local/systemic complications; typically resolves within a week. Moderately Severe AP (MSAP): Characterized by transient organ failure (lasting less than 48 h), local complications, or exacerbation of coexisting diseases. Severe AP (SAP): Defined by persistent organ failure lasting 48 hours or more. b- Systemic Inflammatory Response Syndrome (SIRS) criteria Diagnosis required the presence of two or more of the following. Temperature ( 38c), Pulse > 90/min, Respiratory Rate > 20 or PaCO2  12,000/mm3 or  10% bands. Systemic Inflammatory Response Syndrome (SIRS) criteria Diagnosis required the presence of two or more of the following. Temperature ( 38c), Pulse > 90/min, Respiratory Rate > 20 or PaCO2  12,000/mm3 or  10% bands. c- Bedside Index of Severity in Acute Pancreatitis (BISAP) [ 7 ]:. d- CT Severity Index (CTSI) [ 7 ]: Bedside Index of Severity in Acute Pancreatitis (BISAP) [ 7 ]:. CT Severity Index (CTSI) [ 7 ]: SVT was divided into 3 groups: Portal vein thrombosis (PVT). Splenic vein thrombosis (SpVT). Superior mesenteric vein thrombosis (SMVT). Portal vein thrombosis (PVT). Splenic vein thrombosis (SpVT). Superior mesenteric vein thrombosis (SMVT). SVT was defined radiologically as the presence of: Complete thrombosis (absence of luminal enhancement). Partial thrombosis (non-occlusive hypodense thrombus), Mural thrombosis (wall-adherent thrombus). Complete thrombosis (absence of luminal enhancement). Partial thrombosis (non-occlusive hypodense thrombus), Mural thrombosis (wall-adherent thrombus). Diagnosis was made by contrast-enhanced CT or MRI reviewed by senior radiologists. SVT was assessed on the first CT/MRI systematically performed ≥ 72 h after symptom onset. Additional imaging was performed in cases of clinical worsening, thus allowing consistent detection timing across patients. Statistical analyses were performed using IBM SPSS Statistics version 20. Continuous variables were expressed as means ± standard deviations (SD) or medians with interquartile ranges (IQR), depending on their distribution, and were analyzed using the Student’s t-test or the Mann–Whitney U test, as appropriate. Categorical variables were presented as absolute numbers and percentages, with comparisons made using the chi-square test. Variables showing a significant association with SVT in univariable analysis were included in multivariable logistic regression models for exploratory purposes only, given the limited number of SVT cases. Results of multivariable analyses were interpreted cautiously and considered hypothesis-generating rather than confirmatory.

A total of 402 patients admitted with acute pancreatitis were included in the analysis. The mean age of the cohort was 55.95 ± 18.62 years (range 16–98 years), and there was a female predominance, with 286 women (71.1%) and 116 men (28.9%). Biliary lithiasis was the leading etiology, accounting for 76.1% of cases. Other causes included post-endoscopic retrograde cholangiopancreatography pancreatitis (3.5%), drug-induced pancreatitis (3.0%), hypertriglyceridemia (1.7%), hypercalcemia (1.2%), and chronic alcohol consumption (1.5%). Additional etiologies represented 6.8% of cases, while idiopathic pancreatitis accounted for 6.2% (Table  1 ). Table 1 Baseline characteristics of the study population Variable Number Percent % Age: mean & SD: 55.95 ± 18.6 Gender  Female  Male 286 116 71.1 28.9 Etiologies  Biliary  Post-ERCP  Drug-induced  Hypertriglyceridemia  Hypercalcemia  Alcohol consumption  Other  Idiopathic 306 14 12 7 5 6 24 28 76.1 3.5 3 1.7 1.2 1.5 6.5 6.8 Severity  Mild  Moderately severe  Severe 273 59 70 68 14.6 17.4 Splanchnic venous thrombosis  No  Yes 380 22 94.5 5.5 Pleural effusion :  No  Yes 314 57 85.8 14,2 CTSI (3–10 Pts)  No  Yes 238 164 59.2 40.8 BISAP score (3–5 Pts)  No  Yes 338 64 84.1 15.9 SIRS  Absent  Present  Persistent > 48 H 273 59 70 67.9 14.7 17.4 Death  No  Yes 384 19 95.3 4.7 WON  No  Yes 367 35 91.6 8.4 Pseudocyst  No  Yes 394 8 98.1 1.9 Abbreviations: AP  Acute Pancreatitis, ERCP  Endoscopic Retrograde Cholangiopancreatography, CTSI CT Severity Index, BISAP  Bedside Index for Severity in Acute Pancreatitis, SIRS  Systemic Inflammatory Response Syndrome, WON  Walled-Off Necrosis Baseline characteristics of the study population Female Male 286 116 71.1 28.9 Biliary Post-ERCP Drug-induced Hypertriglyceridemia Hypercalcemia Alcohol consumption Other Idiopathic 306 14 12 7 5 6 24 28 76.1 3.5 3 1.7 1.2 1.5 6.5 6.8 Mild Moderately severe Severe 273 59 70 68 14.6 17.4 No Yes 380 22 94.5 5.5 No Yes 314 57 85.8 14,2 No Yes 238 164 59.2 40.8 No Yes 338 64 84.1 15.9 Absent Present Persistent > 48 H 273 59 70 67.9 14.7 17.4 No Yes 384 19 95.3 4.7 No Yes 367 35 91.6 8.4 No Yes 394 8 98.1 1.9 Abbreviations: AP  Acute Pancreatitis, ERCP  Endoscopic Retrograde Cholangiopancreatography, CTSI CT Severity Index, BISAP  Bedside Index for Severity in Acute Pancreatitis, SIRS  Systemic Inflammatory Response Syndrome, WON  Walled-Off Necrosis According to the Revised Atlanta Classification, most patients presented with mild acute pancreatitis (67.9%), whereas 14.7% were classified as moderately severe and 17.4% as severe disease. Systemic inflammatory response syndrome was absent or transient in the majority of patients; however, 14.7% developed non-persistent SIRS and 17.4% experienced persistent SIRS lasting more than 48 h. A BISAP score greater than 2 was observed in 15.9% of patients, and 40.8% had a CT Severity Index (CTSI) score ≥ 3 (Table  1 ). Regarding local and systemic complications, walled-off necrosis was identified in 8.4% of patients, pseudocysts in 1.9%, infected necrotic collections in 0.8%, and pseudoaneurysms in 0.5%. Ascites and pleural effusion were observed in 13.4% and 14.7% of cases, respectively. The overall in-hospital mortality rate was 4.7% (Table  1 ). SVT was identified in 5.5% of patients ( n  = 22) and involved either a single or multiple venous segments. Among patients with isolated SVT, the most frequent subtype was PVT (38.1%), followed by SMVT (23.8%) and SpVT (19%). In cases of combined SVT, the most frequent association was PVT + SpVT (9.5%), followed by PVT + MSVT (4.8%) and MSVT + SpVT (4.8%). The mean age of patients with SVT was slightly higher (57.32 years) compared with those without SVT (55.87 years), with no statistically significant difference ( p  = 0.723). No significant association was found between gender and the occurrence of SVT ( p  = 0.424). Furthermore, regarding comorbidities, no significant associations were found between SVT and hypertension, diabetes, heart disease, or dyslipidemia. However, SVT was more frequent in patients with a prior history of AP (13.6%) compared to 5% in those without prior AP, although this trend did not reach statistical significance ( p  = 0.08). Clinical presentation differed between patients with and without SVT. Dyspnea was reported more frequently among patients with SVT (9.1%) compared with those without SVT (2.4%), although this difference did not reach statistical significance ( p  = 0.06). Fever occurred significantly more often in the SVT group (31.8% vs. 13.2%, p  = 0.015). Physiological parameters were also higher in patients with SVT. Mean heart rate was significantly elevated (93 ± 17 bpm vs. 82 ± 16 bpm; 95% CI: −17.76 to − 3.67; p  = 0.003), as was respiratory rate (19 ± 4 vs. 16 ± 3 cycles/min; p  = 0.003). In addition, hospitalization duration was longer among patients with SVT (median 14 days vs. 9 days; p  < 0.05). Several laboratory parameters differed between groups (Table  2 ). Patients with SVT demonstrated significantly higher urea levels (0.63 vs. 0.33 g/L, p  = 0.001), elevated C-reactive protein concentrations (191 vs. 133 mg/L, p  = 0.015), and increased white blood cell counts (13,854 vs. 11,343 cells/mm³, p  = 0.034). Albumin levels were significantly lower among SVT patients (31.82 vs. 36.12 g/L, p  = 0.001), and platelet counts were modestly reduced (210,454 vs. 251,942 cells/mm³, p  = 0.045). Creatinine levels did not differ significantly between groups ( p  = 0.723). Table 2 Association between SVT and demographic, clinical, and laboratory characteristics Parameter Without SVT With SVT p -value Age (years), mean ± SD 55.87 ± ? 57.32 ± ? 0.723 Gender (Male %) — — 0.424 History of AP (%) 5% 13.6% 0.08 Dyspnea (%) 2.4% 9.1% 0.06 Fever (%) 13.2% 31.8% 0.015 Heart rate (bpm) 82 ± 16 93 ± 17 0.003 Respiratory rate (cycles/min) 16 ± 3 19 ± 4 0.003 Length of hospital stay (days) 9 14 < 0.05 Creatinine (mg/L) 9 ± 11 9.91 ± 7 0.723 Urea (g/L) 0.33 ± 0.35 0.63 ± 0.88 0.001 Total cholesterol (g/L) 1.5 ± 1.9 1.2 ± 0.5 0.404 Triglycerides (g/L) 1.2 ± 1.5 1.8 ± 3.2 0.122 CRP (mg/L) 133 ± 107 191 ± 100 0.015 Albumin (g/L) 36 ± 5 31 ± 7 0.001 WBC (/mm³) 11,343 ± 5,302 13,854 ± 6,822 0.034 Platelets (/mm³) 251,942 ± 92,713 210,454 ± 113,588 0.045 Procalcitonin (µg/L) 4.4 ± 15 5.7 ± 14 0.714 Abbreviations: SVT  Splanchnic Venous Thrombosis, AP  Acute Pancreatitis, CRP  C-reactive Protein, WBC  White Blood Cells Association between SVT and demographic, clinical, and laboratory characteristics Abbreviations: SVT  Splanchnic Venous Thrombosis, AP  Acute Pancreatitis, CRP  C-reactive Protein, WBC  White Blood Cells SVT occurrence was strongly associated with markers of disease severity. Severe acute pancreatitis was more frequent among patients with SVT than among those without (50% vs. 15.5%, p  = 0.006). Persistent systemic inflammatory response syndrome lasting more than 48 h was also significantly more common in the SVT group (50% vs. 15.5%, p  < 0.001). Higher severity scores were observed among affected patients: BISAP scores greater than 2 were recorded in 31.8% of SVT cases compared with 15% of non-SVT cases ( p  = 0.036), and CTSI scores ≥ 3 were present in 68.2% versus 39.2%, respectively ( p  = 0.007). Local complications were more frequent in patients with SVT (Table  3 ). Walled-off necrosis occurred in 40% of SVT patients compared with 6.6% of those without SVT ( p  < 0.001). Aneurysms were also more common in the SVT group (3.5% vs. 0.3%, p  = 0.006). Ascites and pleural effusion were observed significantly more frequently among SVT patients (40.9% vs. 11.8%, p  < 0.001; and 36.4% vs. 13.4%, p  = 0.003, respectively). Table 3 comparison of severity and local complication between patients with and without SVT Parameter Without SVT (%) With SVT (%) p -value Atlanta Score  MAP 68 30 0.006  MSAP 16.5 20  SAP 15.5 50 SIRS  No SIRS 70.0 31.8  2 15.0 31.8 0.036  CTSI  Score < 3 60.8 31.8 0.007  Score ≥ 3 39.2 68.2  Aneurysms 0.3 3.5 0.006  Ascites 11.8 40.9 < 0.001  Pleural Effusion 13.4 36.4 0.003  WON 6.6 40.0 < 0.001 Abbreviations: MAP  Mild Acute Pancreatitis, MSAP  Moderately Severe Acute Pancreatitis, SAP  Severe Acute Pancreatitis, SIRS  Systemic Inflammatory Response Syndrome, CTSI  CT Severity Index, WON  Walled-Off Necrosis comparison of severity and local complication between patients with and without SVT Abbreviations: MAP  Mild Acute Pancreatitis, MSAP  Moderately Severe Acute Pancreatitis, SAP  Severe Acute Pancreatitis, SIRS  Systemic Inflammatory Response Syndrome, CTSI  CT Severity Index, WON  Walled-Off Necrosis No statistically significant difference in in-hospital mortality was observed between patients with and without SVT (4.5% vs. 4.7%, p  = 0.96). Biliary etiology was the most common in both groups, with 77.9% of patients without SVT and 45.5% with SVT. Alcoholic pancreatitis was more frequent in the SVT group (9.1% vs. 1.1%). Similarly, hypertriglyceridemia, drug-induced pancreatitis, and COVID-19-related pancreatitis were more common in the SVT group (4.5% vs. 1.6%, 4.5% vs. 2.9%, and 4.5% vs. 0.5%, respectively) ( p  = 0.002). Variables that were statistically significant in univariable analyses were entered into a multivariable logistic regression model. Given the limited number of SVT events, this modelling was conducted for exploratory and hypothesis-generating purposes only, and the results should be interpreted with caution. Within this framework, the presence of systemic inflammatory response syndrome remained associated with SVT occurrence (OR = 2.59, 95% CI: 1.89–3.56, p  = 0.006). A CT Severity Index score ≥ 3 was also associated with SVT (OR = 1.74, 95% CI: 1.10–2.74, p  = 0.025). Higher BISAP scores showed a statistical association with SVT (OR = 0.87, 95% CI: 0.84–0.95, p  = 0.005), as did the presence of walled-off necrosis, which demonstrated the strongest relationship (OR = 4.15, 95% CI: 2.56–6.78, p  < 0.001). In addition, elevated CRP levels were associated with SVT occurrence (OR = 1.003, 95% CI: 1.001–1.005, p  = 0.011), and pancreatitis etiology showed a significant association within the model (OR = 7.44, 95% CI: 3.20–17.34, p  = 0.001). In this cohort, 45% of patients diagnosed with splanchnic vein thrombosis received therapeutic anticoagulation. Treatment strategies were heterogeneous and reflected routine clinical decision-making rather than a standardized protocol. The agents used included low-molecular-weight heparin in 30% of treated patients, vitamin K antagonists in 40%, and direct oral anticoagulants in 30%. Anticoagulation was initiated after a mean delay of 5 days following SVT diagnosis (range 2–10 days). Low-molecular-weight heparin was administered as enoxaparin at 1 mg/kg twice daily. Vitamin K antagonists consisted of warfarin with dose adjustment to maintain an INR between 2 and 3. Direct oral anticoagulants included rivaroxaban (15–20 mg/day) or apixaban (5 mg twice daily), prescribed according to renal function and institutional practice. The mean duration of therapy was 4 months, ranging from 3 to 9 months. No clinically documented bleeding events, including gastrointestinal or other hemorrhagic complications, were identified in the medical records of patients receiving anticoagulation during the observation period. However, bleeding outcomes were not prospectively defined using standardized classifications, and event ascertainment relied on retrospective chart review. Therefore, the absence of reported events should not be interpreted as evidence of treatment safety, particularly given the limited sample size. Radiological evolution was assessed using follow-up imaging. In addition to clinically indicated examinations, a systematic cross-sectional imaging assessment was performed at approximately 6 months after diagnosis, allowing standardized evaluation of thrombus evolution. Outcome definitions were standardized across the study: portal cavernoma was defined as the presence of a porto-portal collateral network consistent with chronic portal vein obstruction, whereas chronic thrombosis was defined as persistent thrombus within the splanchnic vein on imaging after 6 months. Recanalization occurred in 66.7% of patients who did not receive anticoagulation, whereas 33.3% developed portal cavernoma. Among treated patients, 55.6% experienced recanalization and 44.4% progressed to chronic thrombosis. Statistical comparison did not demonstrate a significant association between anticoagulation exposure and SVT evolution (Table  4 ). Table 4 SVT Evolution: Comparison of Results With and Without Curative Anticoagulation SVT Evolution Without Curative Anticoagulation (%) With Curative Anticoagulation (%) Recanalization of SVT 66.7 55.6 Portal Cavernoma 33.3 44.4 SVT Evolution: Comparison of Results With and Without Curative Anticoagulation These findings should be interpreted with considerable caution. Treatment allocation was non-randomized and likely influenced by clinical severity and perceived thrombotic risk, introducing potential confounding by indication.

SVT is an uncommon but significant complication of acute pancreatitis, closely associated with disease severity and local complications. Due to the limited number of SVT cases, particularly among anticoagulated patients, conclusions regarding treatment efficacy remain preliminary. Larger prospective studies are needed to better define the role of anticoagulation in this setting.

SVT is a frequent complication of AP, which may develop during the first episode of pancreatitis, either at initial presentation or during the course of treatment [ 9 ]. The prevalence of SVT in our cohort was 5.5%, which aligns with previously reported rates ranging from 0.3% to 62% in AP [ 10 ]. This variability in incidence is mainly due to some factors such as: (1) the heterogeneity in disease severity within the studied populations [ 11 ], (2) the lack of a consensus definition for SVT, which sometimes includes sub-occlusive veins [ 12 , 13 ], 3), the limited literature, consisting mainly of monocentric, retrospective studies with low evidence quality [ 14 ]. According to the largest available retrospective cohort study by Harris et al., SVT primarily affects the splenic vein (67%), followed by the portal vein (52%) and the superior mesenteric vein (38%) [ 15 ]. The development of SVT in AP is primarily driven by Virchow’s triad, which includes venous stasis, endothelial injury, and hypercoagulability. Venous stasis results from extrinsic compression by pancreatic edema and necrotic collections, while endothelial injury is caused by local inflammation and cytokine-mediated damage. Hypercoagulability in AP is attributed to systemic inflammatory activation of the coagulation cascade, as evidenced by elevated D-dimer and fibrinogen levels in SVT patients [ 9 , 16 , 17 ]. Patients with AP are not only at an increased risk of SVT but also other thromboembolic complications like deep venous thrombosis and pulmonary thrombosis [ 18 ]. Complications of SVT include mesenteric ischemia, with an incidence of 4.4% to 16.6% in AP and a mortality rate up to 60%, portal hypertension with an incidence of 15% to 30%, this condition increases the risk of esophageal, gastric varices, ascites, and splenomegaly [ 19 , 20 ]. In our study, we found a significant correlation between SVT and adverse clinical outcomes. This relationship was evident through extended hospital stays, elevated severity scores including SIRS, BISAP, and CTSI and increased levels of inflammatory biomarkers, pleural effusions, and local complications. Previous research has similarly identified a link between SVT and longer hospitalization, as well as a higher likelihood of requiring invasive interventions [ 21 , 22 ]. Our findings align with existing literature that associates the presence, location, and extent of necrosis, along with infections of walled-off necrosis (WON), with the incidence of SVT [ 14 , 23 , 24 , 25 ]. Nawacki et al. further illustrated that the occurrence of SVT is correlated with disease severity: none of the patients with MAP had SVT, while nearly half (46.7%) of patients with MSAP had splenic vein thrombosis and all (100%) had mesenteric vein thrombosis. Among those with SAP, more than half (53.3%) had splenic vein thrombosis and 62.5% had portal vein thrombosis [ 12 ]. Despite its association with increased morbidity, SVT did not significantly affect overall mortality in our cohort. This is in contrast to findings by Nawacki et al. who reported higher mortality rates in SVT patients, albeit not directly attributable to thrombotic complications [ 26 ]. The benefits of anticoagulation in SVT secondary to AP remain controversial, with conflicting evidence in the literature. In our study, 45% of SVT patients received anticoagulation, but no significant difference in recanalization rates or SVT progression was observed between treated and untreated patients. This aligns with a recent meta-analysis that found no clear benefit of anticoagulation on recanalization or prevention of portal cavernoma [ 6 ]. Patients with SVT who may be eligible for curative anticoagulation are often those with SAP, and they are statistically associated with an increased risk of hemorrhagic complications [ 12 ]. Due to the low quality and heterogeneity of studies, the evidence on anticoagulation in AP is limited. Meta-analyses have yielded conflicting results, Some studies indicate that there is no benefit to anticoagulation, while others advocate for its use (Table  5 ) [ 27 , 28 ]. Table 5 Comparison of SVT Rates, anticoagulation, and recanalization in different studies Study % of SVT % of Anticoagulation (AC) Recanalization (AC vs. No AC) Development of Portal Cavernoma (AC vs. No AC) % Hemorrhage (under AC) Charlotte Garret et al. (2018) [ 21 ] 51.7% 51.3% 32% 68% 17% Gonzalez et al. (2011) [ 12 ] 15.7% 20% 50% 50% 0% Laurence Toqué et al. (2015) [ 30 ] 6% 78.9% 47.4% 40% - Our Study (2025) 5.5% 45% 55.6% 44.4% 0% Abbreviations: SVT  Splanchnic Venous Thrombosis, AC  Anticoagulation Comparison of SVT Rates, anticoagulation, and recanalization in different studies Laurence Toqué et al. (2015) [ 30 ] Abbreviations: SVT  Splanchnic Venous Thrombosis, AC  Anticoagulation Regarding guidelines for managing SVT related to AP. The Chinese Society of Gastroenterology provides several recommendations, including proactive anticoagulant treatment for patients with SVT extending to the mesenteric vein and showing clinical signs of intestinal ischemia. Various anticoagulants, such as warfarin, unfractionated. It is recommended to continue anticoagulation for 3 to 6 months, as AP is considered a temporary prothrombotic risk factor. Close monitoring of SVT progression is essential, and anticoagulation should be initiated promptly if the SVT extends in untreated patients [ 29 ]. The guidance issued by the International Society on Thrombosis and Haemostasis recommends consideration of anticoagulation for selected patients with splanchnic vein thrombosis, particularly in the presence of extensive thrombosis or mesenteric involvement, while acknowledging the limited quality of evidence in pancreatitis-related SVT [ 31 ]. Furthermore, higher-level evidence from large systematic reviews and meta-analyses has suggested potential benefits of anticoagulation in SVT, including improved recanalization rates and reduced thrombus progression [ 32 ]. Accordingly, our results should be interpreted as reflecting real-world clinical practice patterns rather than challenging existing evidence. Instead, they highlight the heterogeneity of anticoagulation use in pancreatitis-associated SVT and underscore the need for prospective studies specifically targeting this clinical subgroup. The clinical implication is therefore not to discourage anticoagulation, but to emphasize the uncertainty that persists in its application within this context. The study not only analyzes the prevalence of SVT in AP but also explores its relationship with disease severity and the role of anticoagulation, filling gaps left by previous research. It includes patients from all stages of AP severity, offering a more comprehensive view of SVT prevalence. It is the first to examine the association between SVT and various severity scores of AP, offering unique insights into this complex relationship. The study also addresses important management strategies and patient prognosis, which are key considerations in the treatment of SVT. The study not only analyzes the prevalence of SVT in AP but also explores its relationship with disease severity and the role of anticoagulation, filling gaps left by previous research. It includes patients from all stages of AP severity, offering a more comprehensive view of SVT prevalence. It is the first to examine the association between SVT and various severity scores of AP, offering unique insights into this complex relationship. The study also addresses important management strategies and patient prognosis, which are key considerations in the treatment of SVT. Retrospective, single-center design. Small number of SVT cases, limiting statistical power. Risk of overfitting in multivariable analyses. Inability to draw causal conclusions regarding anticoagulation efficacy. Potential selection bias related to imaging indications and anticoagulation decisions. Retrospective, single-center design. Small number of SVT cases, limiting statistical power. Risk of overfitting in multivariable analyses. Inability to draw causal conclusions regarding anticoagulation efficacy. Potential selection bias related to imaging indications and anticoagulation decisions.

Acute pancreatitis (AP) is a potentially life-threatening inflammatory disorder of the pancreas, characterized by the premature activation of digestive enzymes, leading to autodigestion and tissue damage. This pathology is increasingly prevalent in developed countries, with rising hospitalization rates and potentially severe complications. The primary etiologies include biliary lithiasis (gallstones), chronic alcohol consumption, and metabolic disorders such as hypertriglyceridemia and hypercalcemia [ 1 , 2 ]. AP is associated with a wide range of complications, including pancreatic necrosis, infected necrotic collections, systemic inflammatory response syndrome (SIRS), multi-organ failure, and, in severe cases, mortality [ 3 ]. A frequently underestimated complication of AP is its association with thrombosis, particularly splanchnic vein thrombosis (SVT) [ 4 ]. Thrombosis associated occurs in approximately 22.6% of AP cases and 12.4% of chronic pancreatitis cases, encompassing both systemic and localized thrombotic events [ 5 ]. SVT can lead to severe consequences, including gastrointestinal bleeding, mesenteric ischemia, and complications related to portal hypertension. Despite its clinical relevance, management strategies for SVT in the context of AP remain inconsistent, with studies reporting that up to 53% of patients receive no specific treatment for SVT [ 6 ]. In this study, we aimed to (1) determine the prevalence of SVT among patients hospitalized with AP, (2) evaluate its association with disease severity and clinical outcomes, and (3) describe current management practices, particularly anticoagulation, without inferring treatment efficacy.

Supplementary Material 1. Supplementary Material 1.